Week 1 Flashcards

1
Q

List the main fluid compartments of the human body, and compare their relative magnitude.

A

ICF(half of ECF), ECF(most), Plasma

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2
Q

What 3 conditions are essential to enable the mechanism allowing blood plasma to control the composition of the interstitial fluid?

A

adequate blood flow, small diffusion distance and composition of blood must be controled

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3
Q

What is the general process by which substances are transported between body cells and plasma?

A

diffusion between vessels and cells, transport in blood by convection

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4
Q

Draw a diagram that shows the organs and pattern of blood flow in the pulmonary and systemic circulations.

A

pulmonary and systemic are separate circuits, they are in series while all components in the systemic circulation is in parallel

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5
Q

Define cardiac output and state its approximate magnitude/range in a typical resting individual.

A

volume heart beats in a given time either from right or left ventricle; normally 5L/min

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6
Q

List two important consequences of the parallel arrangement of organs in the systemic circulation.

A

all organs get the same quality blood and volume of blood to each organ can be controlled independently

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7
Q

Explain why the kidneys must receive such a large fraction of the cardiac output.

A

kidneys condition the electrolyte composition of the whole blood system, receive a large amount total cardiac output

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8
Q

Distinguish between organs that are “blood-conditioning” and those that are not, and list some examples of each type.

A

conditioning organs alter the composition of blood for other organs use (kidneys, lungs) others use only for their metabolic needs an are very sensitve to any reduction in flow

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9
Q

Describe the relationship between flow, pressure, and resistance as it relates to a segment of a blood vessel. Write the equation formalizing that relationship.

A

flow equals pressure difference divided by the resistance over a distance (it is pressure gradient, not absolute pressure that determines flow (Q= ΔP/ R)

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10
Q

List the variables that determine resistance to blood flow through a vessel, and write the mathematical formula relating them. Which variable normally plays the most influential role in varying resistance to blood flow?

A

diameter of the vessel, viscosity of blood, length of vessel R= (8Lη)/ (πr^4) Radius has the greatest impact on resistance

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11
Q

Derive the Poiseuille equation and explain its application in the flow of blood

A

Q= ΔP (πr^4/8Lη) combines elements of flow and resistnace equations

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12
Q

How does the pressure gradient between arteries and veins compare between different systemic organs, and what is the main determinant of differences in blood flow between them?

A

gradient between arteries and veins in different systems is similar, the main control of flow comes from the change in the radius of blood vessels/ ie. Changing the vascular resistance

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13
Q

Write the equation that relates cardiac output to the two variables that determine it; list the units of all three quantities.

A

CO = SV x HR : CO [volume/min] = SV [volume/stroke] x HR [beats/minute],

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14
Q

Trace the path of blood flow through the heart, naming all valves that determine the direction of flow.

A

right atrium, tricuspid valve, right ventricles,pulmonary valve, pulmonary circuit, left ventricle, mitral valve, left ventricle, aortic valve, and systemic circulation

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15
Q

Explain what causes the opening and closing of cardiac valves.

A

valves open passively due to pressure differential between atria and ventricle

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16
Q

Define the terms “systole” and “diastole.”

A

systeole (ventricular contraction) diastole (ventricular relaxation)

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17
Q

Define the term “functional syncytium,” and explain how it relates to excitation of the heart.

A

the heart cells are electrically continuous for all purposes which is important for AP conduction and heart rhythm (cells connected by gap junctions)

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18
Q

List the structural components of the heart’s specialized excitation and conduction system, and describe how each functions in the initiation and spread of action potentials through the heart.

A

SA- AV(slowest)- budle of His (only electrical connection between atria and ventricles), Purkinje fibers of the ventricles

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19
Q

List five requirements for effective and efficient operation of the pumping action of the heart.

A
  1. contractions at regular intervals and be synchronized, 2. valves must open fully (not stenotic), 3. valves must not leak (not insufficient), 4. muscle contractions must be forceful (not failing), 5. ventricles must fill adequately during diastole (stretchy compliance is required)
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20
Q

Draw a figure that demonstrates Starling’s Law of the Heart, carefully labeling the axes; then, explain the significance of that relationship for the function of the heart.

A

As cardiac filling increases during diastole, the volume ejected during systole also increases, due to intrinsic property of the heart and primary regulator of cardiac output. Diastolic filling of ventricles determines stroke volume and therefore cardiac output.

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21
Q

Describe the distribution of sympathetic and parasympathetic nerve endings on the heart, list the neurotransmitters and receptors involved, and then describe the effects of each system on the function of the heart.

A

sympathetic system has receptors on both atria and ventricles, through B1 receptors acted on by epi and norepi (heart rate, action potential, conduction velocity, force of contraction rate of contraction and relaxation); parasympathetic only has innervation on the atria to SA and AV nodes release Ach on muscarinic receptors (reduce conduction velocity and force)

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22
Q

List the 5 general blood vessel types blood encounters in the systemic circulation as it passes from left ventricle to right atrium.

A

artery, arteriole, capillary, ventriole, vein

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23
Q

Describe the histological features of the 5 general types of blood vessels, noting which features they have in common and which features distinguish them.

A

arteries (much elastic fibers) arterioles (much smooth muscle) capillaries (very thin lumen), veins and venules (very little muscle, valves very distensible but not elastic therfore hold a lot of blood). All vessels are lined with endothelium with anti-clotting properties

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24
Q

Explain how the anatomy/histology of each systemic vessel type contributes to its main overall function.

A

Arteries: thick walled containing smooth muscle, elastin and collagen fibers (conduit vessels because the have low and unchanging resistance to flow), They have a lot of elasticity, they are considered the highways.

Arterioles: much thicker walls with more smooth muscle (a lot when considering their cross-sectional area) and less elastic material (resistance vessels)

Capillaries smallest vessels consisting of a single layer of endothelial cells and no smooth muscle (exchange vessels), given the example of the tea bag, with diabetes the excess glucose can gum up the basement membrane

Venous vessels have very thin walls in proportion to their diameters, their walls contain smooth muscle and thin walls are very distendible (holds a lot of blood but does not have the elasticity to “snap back” and diameters change in response to transmural distending pressure (capacitance vessels) and chances to venous volume influence cardiac filling and therefore cardiac pumping. (very important for cardiac output)

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25
Q

Detail the 2 mechanisms that control the diameter of arterioles, and the one mechanism that controls the diameter of the veins

A

arterioles: sympathetic and paracrine regulation, veins: sympathetic innervation

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26
Q

. Define the term hematocrit, and give an approximate value in a typical, healthy person.

A

the measure of formed solids (cells) in the blood, normally 40%

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27
Q

List the 3 general types of formed elements in the blood, and state the general function of each.

A

RBC carry oxygen (most abundant), WBC immune function, Platelets clotting

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28
Q

Explain the distinction between plasma and serum

A

Plasma has clotting elements, serum does not

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29
Q

List the solutes found in the plasma component of blood, and note which are present in the highest concentration.

A

sodium, potassium, bicarbonate, chloride, in blood Sodium and chloride are most abundant

30
Q

Describe the composition of isotonic saline, and explain its clinical usefulness

A

saline is both sodium and chloride 150 mM

31
Q

List the 3 categories of plasma proteins, and describe the general function of each category

A

albumin (carrier) immunoglobulins (immune function) fibrinogen (clotting)

32
Q

List some of the organic nutrient and waste molecules dissolved in plasma.

A

amino acids, glucose, urea, creatinine and uric acid

33
Q

List some of the general characteristics of cardiac muscle cells.

A

demonstrate electrical conductance and reliable contractile and pumping characteristics

34
Q

List 3 ways that cardiac cell action potentials differ from skeletal muscle action potentials

A

contraction can be self generating, potentials can be directed from cell to cell, action potentials have long durations

35
Q

Review the following concepts of membrane biophysics: Ion gradients, equilibrium potentials, voltage-gated ion channel activation, ion-channel inactivation, resting membrane potentials, threshold potential, action potentials, absolutely refractory period, relative refractory period.

A

just do it.

36
Q

Draw a typical cardiac muscle cell action potential (fast-response cells), name the phases, and describe the ion-channel events that determine the shape.

A

Fast Response: Phase 4 (resting but changing membrane before AP, T type Ca active) Phase 0 (rising stroke due to fast Na channels opening and inactivating), Phase 1 (transient drop after peak) Phase 2 (AP plateau due to L tyep Ca channels) Phase 3 (down stroke due to K primarily, K is slow to respond)

37
Q

. Draw a typical cardiac muscle cell action potential (fast-response cells), name the phases, and describe the ion-channel events that determine the shape.

A

Fast Response: Phase 4 (resting but changing membrane before AP, T type Ca active) Phase 0 (rising stroke due to fast Na channels opening and inactivating), Phase 1 (transient drop after peak) Phase 2 (AP plateau due to L tyep Ca channels) Phase 3 (down stroke due to K primarily, K is slow to respond)

38
Q
  1. Draw a typical cardiac node cell action potential (slow-response cell), name the phases, and describe the ion-channel events that determine the shape.
A

Slow response: Phase 4 (rising due to funny Na channels and contributing T type Ca) Phase 0-2 mostly due to Ca channels, L type) and Phase 3 (K+ conductance)

39
Q
  1. Describe the structure and function of intercalated disks in cardiac cells.
A

to connect cardiac cells and conduct electrical currents; structures include hemdesmosomes and adherins for connection and conexins in gap junctions to create low resistance connections

40
Q
  1. What three variables determine the variation in action potential conduction velocity in different regions of the heart?
A

Cell diameter (AV node small, Purkinje huge), intensity of depolarizing current (Na+> Ca2+ current), properties of membrane and gap junctions (second messengers, phosphorylation via autonomic receptors (ie. sympathetic

41
Q
  1. Draw a graph demonstrating the spread of an action potential during a single beat of the heart, showing the shapes and relative timing of the action potential in the following cell types: SA node, Atrial muscle, AV node, Purkinje, ventricular muscle
A

action potential is staggered spacially as AP travels through heart; fast cells: earliest to depolarize take the “longest” to depolarize, and the last to depolarize are first to repolarize

42
Q
  1. Explain in a general way what is measured by electrocardiography, and describe what cellular events are indicated by P, QRS, and T-waves.
A

EKG measures the electrical voltage between two points. P wave is atrial depolarization, QRS is ventricle depolarization, T is ventricle repolarization

43
Q
  1. Define automaticity, and describe the cells that are the normal pacemaker of the heart, stating their intrinsic rate of activity.
A

Automaticity: contractions that occur due to spontaneous pacemaker activity SA node 100/min is the normal pacemaker of the heart

44
Q
  1. Describe the cellular mechanisms by which parasympathetic and sympathetic neurons modulate automaticity of the heart.
A

by altering funny Na channel permeability

Acteylcholine released by parasympathetic nerves increase resting K+ permeability and decreases diastolic permeability to Na+ (funny currents) which drives the membrane potential more negative. Parasympathetic also decreases L-type Ca++ current and slow the upstroke, so conduction velocity is decreased in the cells of the atria (negative dromotropic effect- slows contraction speed)

Increasing sympathetic tone results in increases in heart rate while increasing parasympathetic tone decreases heart rate by altering the spontaneous depolarization of the pacemaker cells. This is done by norepi on B1 receptors which increases the funny Na current and Ca++ current (T type so cells reach potential faster). Sympathetic also increase L-type Ca++ current and speeds upstroke.

45
Q
  1. Describe the dromotropic effect of sympathetic and parasympathetic neurons on cells of the AV node, and how that would be expected to alter cardiac function.
A

Dromotropic effect: conduction speed

Parasympathetic linked muscarinic receptors are linked to G inhibitory proteins to increase K+ permeability and decrease cAMP and reduce the inward going pacemaker current. Increased parasympathetic activity has a negative dromotropic effect.

Sympathetic nerves release norepi on B1 adrenergic receptors which are linked to stimulatory G proteins and increase the open state probability in Na+ current channel, increasing the rate of diastolic depolarization. Sympathetic increase AP velocity that has a positive dromotropic effect.
These effects are most apparent at the AV node and affect the PR interval.

46
Q
  1. List the two sources of elevated cytosolic Ca2+ during contraction of cardiac muscle, state which causes the largest change, and explain how elevated Ca2+ leads to force generation.
A

A small change in intracellular Ca++ causes a large amount of Ca++ to be released from the sarcoplasmic reticulum. Ca++ increases the interaction between myosin and actin fibers
Variations in the amount of “trigger” Ca++ and the Ca++ release from the sarcoplasmic reticulum vary cardiac “contractility.”

47
Q
  1. List the three mechanisms that remove Ca2+ from the cytosol of cardiac muscle cells after a contraction, and state the proportion of Ca2+ removed by each mechanism.
A

Active uptake into the Sarcoplasmic reticulum is 80%
Extrusion from the cell by Ca ATPase pumps 5%
Na/Ca++ exchanger 15% (powered by the sodium gradient to remove Ca++ from the cell)

48
Q
  1. Explain how the cardiac glycoside, digitalis, increases contractile force in failing hearts.
A

Cardiac glycoside digitalis slows down the Na/K pump and thus reduces the sodium gradient. Therefore, increased Ca++ is sequestered in the SR and increases contractile force. (Na/K exchanger electrogenic effect also effects the AP plateau)

49
Q
  1. Explain why cardiac muscle cells cannot undergo fused tetanic contractions like those occurring in skeletal muscle cells.
A

The contraction of cardiac muscle lasts as long as the action potential that caused it so there is no way to summate AP and contractile force. The cell cannot be activated fast enough to induce fused tetany.

50
Q
  1. Differentiate between isotonic and isometric contractions of muscle cells.
A

Isotonic is constant tension and varying length, isometric is a muscle that does not change length although it might increase or decrease tension. Heart cells undergo isometric contraction before valves open and isotonic after valves open

51
Q
  1. Draw a graph that shows the effect of increasing muscle length on resting muscle tension, active isometric muscle tension, and total muscle tension. Compare the length at which cardiac muscle normal operates, to the length on this graph where active tension is greatest (Lmax).
A

cardiac muscle operates normally way below the Lmax, therefore increasing the muscle length increases the tension developed

52
Q
  1. Describe the contractile behavior that occurs when cardiac muscle contractile potential is greater than the load it contracts against.
A

. It will cause the muscle to contract isotonically and shorten. It will shorten until the muscles tension producing potential is decreased sufficiently by the length change to be equal to the load on the muscle

53
Q
  1. Using a graph of muscle length vs muscle tension, differentiate between the contractile behavior of a muscle undergoing an isotonic contraction from a muscle undergoing an afterloaded contraction.
A

Preload stretches the ventricle then the ventricle isometrically contracts until meets the pressure of the valves (afterload) and isometricaly contracts until valves open and then isotonic contraction resumes

54
Q
  1. State the distinguishing feature of an intervention that alters “contractility” of heart muscle.
A

Any intervention that that increases the peak isometric tension that a muscle can develop at a fixed length is said to increase the cardiac muscle contractility

55
Q
  1. Draw a figure that demonstrates the effect of norepinephrine from sympathetic nerves on the contractility of cardiac muscle, differentiating between the effect on isometric and afterloaded contractions.
A

norepinephrine can affect the afterload in that it causes the cardiac muscle to shorten a greater distance than it would normally, it also increases the maximal isometric tension

56
Q
  1. Detail the cellular mechanisms coupling norepinephrine binding to the positive inotropic and positive lusitropic effects on cardiac muscle cells.
A

G protins linked to a B1 receptor activates PKA to alter the action of calcium channels on the sarcoplasm and the sarcoplasmic reticulum; Inotropic: increases activity of Ltype Ca++ channels and affects ryanodine receptors which loads ERs (faster depolarization) Phosphorylation of phospholamban on the SR Ca ATPase increases the rate of calcium retrapping and decreases the action potential length—leads positive lusitrophic efffect

57
Q
  1. Explain how changes in heart rate directly contribute to changes in cardiac muscle contractility.
A

inotropic effects on the heart during increased heart rate will lead to greater Ca++ in the cell and lusitropic effects will lead to faster relaxation, so overall a quicker contraction

58
Q
  1. Describe three critical functional implications that arise from the fact that ventricular muscle cells are oriented circumferentially in the ventricular wall.
A
  1. increase in ventricular volume increases ventricular circumference and thus the diastolic filling of the ventricle determines the preload
  2. At any ventricular volume, an increase in the tension of individual cardiac muscles cells causes an increase intravetricular pressure
  3. As ventricular volume decreases a lesser total force is required by the muscle cells in the ventricular walls to produce any give intraventricular pressure.
59
Q
  1. Write the equation that expresses the law of Laplace, and explain how it applies to ventricular function.
A

T= Px r the relationship between total wall tension and internal pressure in a hollow vessel with circular containing walls depends on the intraventricular pressure and its internal radius. One application of this is that the muscle cells in the ventricular wall have an easier job producing internal pressure at the end of systole and significance in other pathological conditions. Dialated hearts (increased r) require more tension to generate a given pressure)

60
Q
  1. Draw one comprehensive graph that shows the phases of a single cardiac cycle for the left side of the heart, relating the following cardiac variables over time: Lead 2 ECG, Muscle contraction, aortic pressure, left ventricular pressure, left atrial pressure, aortic and mitral valve opening/closing, heart sounds, left ventricular volume, and aortic blood flow. Be able to explain the causal and temporal relationships among all of these variables.
A

practice starting with the closing of the mitral valve. Include verticle lines that denote diastole and the 3 phases of systole

61
Q
  1. Explain the major differences between the events described in the last question for the left side of the heart, and those same events as they occur in the right side of the heart.
A

Have same stroke volume, under same electrical control, right side is generally at a lower pressure. Pressures developed are considerably lower than that of the ventricles, the magnitude of the peak systolic pressure is much less in the atria (there is much less resistance in the pulmonary circuit

62
Q
  1. List the 3 components of the jugular vein pulse, and explain the cause of each component.
A

A wave, atrial wave produces the first pressure peak (atrium contracts)
C wave follows shortly after due to the onset of ventricular systole and by an initial bulging of the tricuspid valve into the right atrium (ventricle contracts)
V wave, increased pressure as the central veins and right atrium fill behind a closed tricuspid valve with blood returning to the heart (atrium fills)

63
Q
  1. Draw a graph showing the changing relationship between intraventricular volume and intraventricular pressure during a single cycle of the heart. Label the cardiac phases and note the points at which cardiac valves open and close.
A

isometric contraction of ventricle until overcomes after load volume, then isometric contraction to move blood out of heart. then isovolumetric relaxation and passive stretching during filling

64
Q
  1. Define ventricular preload and ventricular afterload.
A

Ventricular preload is the ventricle loaded with blood and the pressure that puts on the ventricle and ventricular afterload is additional pressure that the aortic pressure adds against the contracting ventricle—important for opening of aortic valve (a range of values)

65
Q
  1. Draw two superimposed ventricular pressure-volume loops that demonstrate the effect of preload on stroke volume.
A

greater preload results in greater stroke volume with no change in end diastolic volume

66
Q
  1. Draw two superimposed ventricular pressure-volume loops that demonstrate the effect of afterload on stroke volume.
A

greater afterload results in less cardiac muscle shortening, after resulting in reduced stroke volume and increased end-systolic volume

67
Q
  1. Draw two superimposed ventricular pressure-volume loops that demonstrate the effect of changes in cardiac muscle contractility on stroke volume.
A

contractility increases stroke volume, greater end diastolic volume can stretch cardiomyocytes and increase contractility along with NE or Epi

68
Q
  1. Summarize the effects of cardiac parasympathetic nerve activity level, cardiac sympathetic nerve activity level, arterial pressure, and filling pressure on 1)heart rate, 2) stroke volume, and 3) cardiac output.
A

Ach on muscarinic receptors decreases peak isometric tension and amount of shortening at any length, at a given preload, decreases rate of pressure development and SV, emptying of heart to a larger end systolic volume

69
Q
  1. Draw and explain a graph showing the effect of sympathetic nerve activity level on the relationship between cardiac filling pressure and cardiac output.
A

increasing preload leads to more shortening cardiomyocytes

70
Q
  1. Define angina pectoris, and describe its direct and indirect causes.
A

Severe chest pain or discomfort due to a mismatch in the metabolic requirements of the heart and what is supplied by the coronary arteries, due to cardiac ischemia